Abstract / Summary
Sclerotinia sclerotiorum is a necrotrophic fungus that causes severe plant diseases but can also colonize wheat as a symptomless endophyte. However, the mechanism by which its effector proteins regulate this dual lifestyle remains unclear. This study aimed to identify key LysM effectors involved in S. sclerotiorum-plant interactions and elucidate their specific functions. Among seven SsLysM genes, SsLysM6 and SsLysM7 were transcriptionally upregulated during both the pathogenic infection of rapeseed and the endophytic colonization of wheat. The ΔSsLysM6 and ΔSsLysM7 mutants exhibited significantly reduced colonization abilities on both their pathogenic host (rapeseed) and their endophytic host (wheat). Transient expression of SsLysM6 and SsLysM7 in Nicotiana benthamiana leaves demonstrated that both effectors suppress chitin-induced immune responses, including reactive oxygen species (ROS) bursts, MAPK activation, and immune gene expression. Recombinant SsLysM6 and SsLysM7 proteins exhibited chitin-binding ability and efficiently suppressed chitin-triggered ROS bursts in wheat leaves. These findings provide critical insights into the molecular mechanism by which S. sclerotiorum establishes compatible interactions across genetically diverse hosts, highlight the central role of LysM effectors in fungal adaptation to distinct lifestyles, and offer new perspectives on the evolutionary continuum between pathogenic and endophytic fungi.